支原体脂肽经TLR2,6/c-Src/PI3K通路诱导单核细胞表达血红素氧合酶-1  

A mycoplasma lipopeptide induces hemeoxygenase-1 expression via TLR2, 6/c-Src/PI3K pathway in monocytes

作　　者：游晓星[1] 马小华[2] 刘良专[1] 曾焱华[1] 朱翠明[1] 何军[3] 蒋传好[1] 吴移谋[1] 

机构地区：[1]南华大学病原生物学研究所,衡阳421001 [2]长沙市中心医院,长沙410004 [3]南华大学附属南华医院,衡阳421001

出　　处：《中国免疫学杂志》2014年第5期587-590,共4页Chinese Journal of Immunology

基　　金：国家自然科学基金(31000091;81072418);湖南省高校科技创新团队资助项目(湘教通[2010]212号);湖南省研究生培养创新基金资助项目(湘教通〔2008〕249号)

摘　　要：目的:观察支原体巨噬细胞活化脂肽2(Macrophage-activating lipopeptide-2,MALP-2)诱导人单核细胞系THP-1表达血红素氧合酶-1(Hemeoxygenase,HO-1)的分子机制。方法:体外培养THP-1细胞,用不同浓度的MALP-2作用12 h,Western blot检测HO-1的表达。THP-1细胞经TLR2和TLR6中和抗体孵育,或构建TLR2和TLR6负显性突变体转染细胞,以明确TLR2和TLR6在介导HO-1表达中的作用;Western blot检测c-Src和Akt磷酸化情况,同时,分别采用c-Src siRNA或PI3K抑制剂LY294002处理细胞,观察c-Src及PI3K在HO-1表达中的作用。结果:MALP-2处理后可磷酸化c-Src,而TLR2和TLR6中和抗体以及其负显性突变体转染后,c-Src磷酸化水平显著降低;同时,c-Src siRNA可降低Akt磷酸化水平,而PI3K抑制剂LY294002处理后可明显降低HO-1的表达。结论:MALP-2能诱导THP-1细胞表达HO-1,其机制可能受TLR2,6/c-Src/PI3K通路调控。Objective：To observe the molecular mechanism involved in expression of hemeoxygenase -1 （HO-1） induced by a macrophage-activating lipopeptide-2 （MALP-2）.Methods：THP-1 cells were cultured in vitro and stimulated by MALP-2 for 12 h, expression of HO-1 was detected by Western blot .TLR2 and TLR6 neutralizing antibodies incubation , dominant negative plasmids transfection were used to assess the functional of TLR 2,6 in mediating HO-1 expression.Phosphorylation of c-Src and Akt were detec-ted by Western blot, and c-Src siRNA and PI3K inhibitor LY294002 were used to investigate the role of c-Src and PI3K in HO-1 ex-pression.Results：MALP-2 induced c-Src phosphorylation , and TLR2 and TLR6 neutralizing antibodies , or their dominant negatively plasmids could abrogate this effect .In addition, siRNA of c-Src could decrease the phosphorylation level of Akt , and the PI3K inhibi-tor could inhibit HO-1 expression.Conclusion： MALP-2 can induce THP-1 cells expression of HO-1 through TLR2,6/c-Src/PI3K pathways .

关 键 词：支原体巨噬细胞活化脂肽2 血红素氧合酶-1 单核细胞 

分 类 号：R392.9[医药卫生—免疫学]